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Nutrition and Experimental Carcinogenesis: a Review'

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Nutrition and Experimental Carcinogenesis: a Review' [CANCER RESEARCH 35, 3292-3300November 1975] Nutrition and Experimental Carcinogenesis: A Review' David B. Clayson Eppley Institute for Research in Cancer, University of Nebraska Medical Center, Omaha, Nebraska 68105 Summary considerably modify the response of experimental animals in carcinogenicity tests. Restriction of the total diet or the number of calories fed Changes in tumor incidence may also be brought about to rats and mice inhibits the formation of tumors in several by altering the composition of the diet. In some cases, tissues. Unless animals are fed equivalent levels of food, or especially in that of chemical carcinogens, there is knowl attain equivalent body weights, it is difficult to assess the edge of the mechanism by which these changes arise. significance of the effect of other nutritional modifications Modifications of the metabolic activation of carcinogens by on carcinogenesis. The effects of altering the levels of controlling the levels of cofactors or by inducing different protein or fat are much less than those seen with dietary patterns of metabolizing enzyme activities are well docu restriction. Feeding a protein-free diet is tolerated for a mented. On the other hand, those factors which regulate limited period and can alter the metabolism of carcinogens. tumor development, such as different levels of cellular It may thus affect the tumor incidence induced by one-shot proliferation or immunological control, do not appear to carcinogens. Vitamins have specific effects on the activity of have been as amenable to study. certain carcinogens, the fullest information being available This presentation will illustrate the way in which nutni for vitamin A, which has been shown to inhibit or enhance tional differences can affect tumor incidence in experimen carcinogenesis, and vitamin C, which by reducing sodium tal systems. Wherever possible, the mechanism by which nitrite, prevents nitrosation of secondary and tertiary these changes are mediated will be discussed. amines occurring in acidic conditions of the stomach. Inorganic substances, such as iodine (thyroid) and copper Dietary and Caloric Restriction (liver), may affect the tumor incidence in specific tissues. The metabolic activation of carcinogens is modified by The demonstration from actuarial records that over enzyme induction and the administration of antioxidants. weight or obese men had a higher cancer mortality than The relevance of these results to the induction of cancer in normal or underweight men led Tannenbaum (93) to humans is briefly discussed. investigate the effect on the development of spontaneous and induced tumors of a restricted dietary intake in mice. Introduction Dietary restriction reduced the incidence of mammary tumor virus-induced tumors in DBA and C3H mice, Carcinogenesis may be affected by nutrition in 2 ways. spontaneous lung tumors in Swiss and ABC mice, B(a)P Food or drink may be contaminated by carcinogens, or the induced skin tumors and, to a lesser extent, s.c. sarcomas composition of the diet may impose upon the host patterns induced by B(a)P (Chait 1) (94, 95). Similar effects have of enzyme activity and other factors that dictate the yield of been observed in rats. As in mice, underfeeding greatly naturally occurring or induced tumors. The deliberate increased the life-span (45) and led to a lower tumor addition of carcinogenic additives to food should diminish, incidence than that found in animals that received ad as a result of worldwide governmental action. Nevertheless, libitum supplements 74, 80). In these underfeeding studies, the control of naturally occurring carcinogens in food the amounts of the various dietary components were presents difficulties, especially for technically developing reduced proportionately to each other. countries. The most studied naturally occurring carcinogens An alternative to underfeeding is caloric restriction, in include aflatoxins B1 and G1, sterigmatocystin, and other which the amount of carbohydrate is reduced, while other mycotoxins (40). There is presumptive evidence that components are maintained at a constant level. Calorie aflatoxins are carcinogenic in humans (67). Also to be restricted diets also lessen the incidence or delay the considered are the carcinogens present in bracken fern appearance of certain tumors, such as mammary tumors in (20—22,64), cycasin (42), the nitrosamines, especially those DBA mice (Chart 2) (97). In this example, the inhibition formed from nitrite and secondary or tertiary amines (53, was apparent, even if the restricted diet was not instituted 79), environmental goitrogens, and hormones, and other until the mice were 9 months old. dietary carcinogens. Besides their possible carcinogenic The mechanism by which dietary restriction inhibits actions in man, the presence of these substances may 2 The abbreviations used are: B(a)P, benzo(a)pyrene; DAB; 4-dimeth ylaminoazobenzene; DMN, dimethylnitrosamine; MCA, 3-methylcholan CPresentedattheConferenceonNutritionintheCausationofCancer, threne; DMBA, 7,l2-dimethylbenz(a)anthracene;FAA, N-2-fLuorenyl May 19 to 22, 1975, Key Biscayne,Fla. Supported by Contract NOI acetamide;BHA, butylated hydroxyanisole; BHT, butylated hydroxytol CP33278from the National Cancer Institute, NIH, USPHS. uene. 3292 CANCER RESEARCH VOL. 35 Downloaded from cancerres.aacrjournals.org on September 30, 2021. © 1975 American Association for Cancer Research. Nutrition and Experimental Carcinogenesis U) mediated through its effect on body weight. They suggested 0 that the inhibition of tumorigenicity is associated with an D I-. overall nutritional deficiency at the cellular level, but did not 0 Mammary speculate as to the nature of the process. Whatever the SkinTumors Carcinomas explanation of these observations, they are crucial to all 30— (24 weeks) (24 weeks) (86weeks) aspects of experimental tumorigenesis. Experiments de @2O— fl signed to show anything more than the crudest tumor-induc @l:1@J@ L1= EL ing potency of a strong carcinogen must be carried out in such a manner that all experimental and control groups @ :@ DIETadIsbitum maintain similar body weights. Experiments that fail to @@ RestrictedDIET adhere to this principle are difficult to interpret. Factors Chart I . The effect of restricting caloric intake on the incidence of that may lead to decreased body weight in treated animals sarcomas and skin tumors induced by B(a)P and on naturally occurring include chemical toxicity, unpalatability of the diet, and mammary tumors in DBA mice (95). chronic ill health in the colony. Good experimentation can overcome these difficulties. Because the influence of dietary and caloric restriction was not realized until 1940, work in 00 nutrition and cancer carried out before that time is difficult to interpret. 80 U z U a Protein Levels U -p z g 2 A MAMMARY-DBAQMICE The feeding of isocalonic diets containing levels of protein I- B SKIN-B(a)P INDUCED 1e 20- C MAMMARY-C3H9MICE ranging from 9 to 45% failed to influence the incidence of 0- - mammary tumors in DBA and C3H mice, and that of hydrocarbon-induced skin tumors and s.c. sarcomas. Spon ‘ 0 II 2 3 14 CALORIC INTAKE per DAY taneous hepatomas in C3H mice occurred less frequently Chart 2. The effect of caloric restriction on mammary tumor induction when the 9% protein diet was fed (100). This was due to a in C3H and DBA mice and on skin tumors inducedby B(a)P (98). diminution in the concentration of the essential sulfur-con taming amino acids, cysteine and methionine. The addition of sufficient protein, freed from these amino acids, to raise tumonigenesis is unknown. Initiation-promotion studies in the protein level from 9 to 18%, failed to affect the incidence skin carcinogenesis were said to show that restriction was of spontaneous hepatomas, whereas addition of the calcu effective in the promotion or developmental stage of tumor lated amounts of these amino acids did so (88). formation, but some influence on the initiation stage could High protein levels, however, protect the rat liver against not be excluded by the data presented (Table 1) (97). The carcinogenesis by DAB. Adequate dietary casein, even with yield of mammary tumors was not affected by starving low levels of riboflavin (see below) protects the rat liver DBA. mice for 2 periods of 24 hr each week and permitting against this chemical. The reason for this phenomenon is them to eat ad libitum for the remaining time. These mice not known. Tannenbaum and Silverstone (104) suggested consumed as much as those fed ad libitum continuously that the high-protein diet might be protective because it (101). The actual number of calories is not necessarily enabled the liver to store and utilize riboflavin more significant, because mice fed thyroid extract consumed 1.5 efficiently. times the normal amount, while maintaining a slightly lower Ross and Bras (75) fed diets containing 10, 22, or 51% than average body weight. The yield of tumors induced by casein on either a restricted (equicaloric) or an ad libitum painting B(a)P on the skin was unaffected by thyroid extract (85). Other treatments, which did not involve reduction of Table I caloric intake and reduced body weight, included maintain The dependenceof the genesisof induced skin tumors on the caloric ing the mice in a cold environment (7.2—12.8°)or feeding intake during different stages of carcinogenesis° them dinitrophenol or sodium fluoride. Each of these Diet50-wkGrouplO-wk treatments significantly inhibited naturally occurring mam mary tumors in DBA mice. The chemicals blocked forma tion of lung adenomas but had little effect on B(a)P-induced sarcomas, while dinitrophenol showed little influence on painting ment of tumorsIPF49692FR50343RR50244RF5055perioddevelop periodNo. mice% B(a)P-induced skin tumors (99). Gold thioglucose induces a specific hypothalamic lesion in mice which causes severe obesity through an increase in adipose tissue, leading to a doubling of the body weight. A high incidence of mammary tumors were obtained in these animals (113). Tannenbaum and Silverstone (104) concluded that the aFromRef.95 relevant effect of dietary or caloric restriction was probably a F, full diet; R, restricted diet.
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